Requirement of extracellular signal-regulated kinase/mitogen-activated protein kinase for long-term potentiation in adult mouse anterior cingulate cortex.
Requirement of extracellular signal-regulated kinase/mitogen-activated protein kinase for long-term potentiation in adult mouse anterior cingulate cortex.
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DOI：
10.1186/1744-8069-3-36
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发表时间：
2007-12-01
期刊：
影响因子：
3.3
通讯作者：
Zhuo M
中科院分区：
文献类型：
--
作者：
Toyoda H;Zhao MG;Xu H;Wu LJ;Ren M;Zhuo M
前扣带回皮质(ACC)的长时程增强(LTP)被认为对包括情绪、学习、记忆和慢性疼痛在内的高级大脑功能至关重要。依赖N-甲基-D-天冬氨酸(NMDA)受体的LTP被广泛研究，并被认为对哺乳动物大脑的学习和记忆具有重要作用。作为NMDA受体的下游靶点，丝裂原活化蛋白激酶(MAPK)级联中的细胞外信号调节激酶(ERK)参与了海马区突触的可塑性和学习记忆，受到了广泛的研究。相反，ERK在扣带回LTP中的作用尚未被研究。在这项研究中，我们研究了ACC中的LTP是否需要ERK的激活。我们发现，p42/p44 MAPK抑制剂PD98059和U0126抑制了由突触前刺激和突触后去极化(配对方案)诱导的扣带回LTP。我们还发现，另外两种不同方案诱导的扣带回LTP也被PD98059阻断。此外，我们还发现这两种抑制剂对扣带回LTP的维持没有影响。MAPK家族的其他成员c-Jun氨基末端激酶(JNK)和p38的抑制剂SP600125和SB203850可抑制由配对方案产生的扣带状LTP的诱导。因此，我们的研究表明，MAPK信号通路参与了扣带回LTP的诱导，并在生理条件下发挥了关键作用。
Long-term potentiation (LTP) in the anterior cingulate cortex (ACC) is believed to be critical for higher brain functions including emotion, learning, memory and chronic pain. N-methyl-D-aspartate (NMDA) receptor-dependent LTP is well studied and is thought to be important for learning and memory in mammalian brains. As the downstream target of NMDA receptors, the extracellular signal-regulated kinase (ERK) in the mitogen-activated protein kinase (MAPK) cascade has been extensively studied for its involvement in synaptic plasticity, learning and memory in hippocampus. By contrast, the role of ERK in cingulate LTP has not been investigated. In this study, we examined whether LTP in ACC requires the activation of ERK. We found that P42/P44 MAPK inhibitors, PD98059 and U0126, suppressed the induction of cingulate LTP that was induced by presynaptic stimulation with postsynaptic depolarization (the pairing protocol). We also showed that cingulate LTP induced by two other different protocols was also blocked by PD98059. Moreover, we found that these two inhibitors had no effect on the maintenance of cingulate LTP. Inhibitors of c-Jun N-terminal kinase (JNK) and p38, other members of MAPK family, SP600125 and SB203850, suppressed the induction of cingulate LTP generated by the pairing protocol. Thus, our study suggests that the MAPK signaling pathway is involved in the induction of cingulate LTP and plays a critical role in physiological conditions.
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